“…The purported mechanism by which anemia manifests as cribra orbitalia is considered to be, for the most part, compensatory red bone marrow expansion. While there are numerous pathological processes that manifest as anemia, the literature has focused mainly on (a) nutritional anemias—attributed to iron‐deficiency, vitamin B9 deficiency, and/or vitamin B12 deficiency (Carlson et al, 1974; El‐Najjar et al, 1976; Hengen, 1971); (b) anemias induced by parasites—attributed to malaria (i.e., Plasmodium parasites) (Angel, 1966; Blondiaux et al, 2015; Gowland & Western, 2012; Kyle et al, 2020; Smith‐Guzmán, 2015), Ancylostoma duodenalis (Cornero & Puche, 2002), Necator americanus (Cornero & Puche, 2002), or, alternatively, that iron‐deficiency anemia is a host‐generated adaptive response to deprive parasites from the host's iron (Fairgrieve & Molto, 2000; Stuart‐Macadam, 1992); (c) genetic anemias—mainly sickle cell anemia and thalassemia (which, paradoxically, may confer some protection from malaria) (Carlson et al, 1974; Nathan et al, 1966); and (d) a blended form of anemia—for example, an anemia of infection with concomitant iron‐deficiency anemia (Lallo et al, 1977).…”